β-Amyloid Increases Enzyme Activity and Protein Levels of Glutamine Synthetase in Cultured Astrocytes

Pike, Christian J.; Ramezan‐Arab, Nima; Miller, Stephan; Cotman, Carl W.

doi:10.1006/exnr.1996.0091

Cited by 17 publications

(8 citation statements)

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“…In rat cortical cultures, however, aggregated Ab 1-42 peptide stimulated the expression of GS (Pike et al 1996). Hence, the present finding of pro-oxidant diet-enhanced expression of both GS and VGLUT-1 in transgenic mice may reflect a synaptic plasticity response to oxidative stress induced on a background of enhanced APP/Ab expression.…”

Section: Discussioncontrasting

confidence: 43%

Synaptic protein expression is regulated by a pro-oxidant diet in APPxPS1 mice

et al. 2011

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Dietary factors may play a role in Alzheimer's disease (AD) pathogenesis. In an effort to recapitulate some of the synaptic protein changes observed in the disease, AD transgenic and wild-type mice were fed either a normal or pro-oxidant diet for 3 months from three months of age. Pro-oxidant diet treatment resulted in altered expression of vesicular glutamate transporter-1 and glutamine synthetase, suggesting changes in glutamatergic synaptic function, and increased expression of urokinase plasminogen activator receptor, possibly reflecting oxidative stress.

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Section: Discussioncontrasting

confidence: 43%

Synaptic protein expression is regulated by a pro-oxidant diet in APPxPS1 mice

et al. 2011

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“…This finding suggests that the aggregated A␤ in plaques is not directly responsible for the suppression of GS expression in AD. This suggestion is further supported by the in vitro observation that aggregated A␤ peptides actually stimulate an increased expression of GS in cultured rat astrocytes (Pike et al, 1996). These findings are inconsistent with the above-mentioned biochemical data and the results from cortical homogenates.…”

mentioning

confidence: 54%

Changes in the cellular distribution of glutamine synthetase in Alzheimer's disease

Robinson

2001

J of Neuroscience Research

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The intracellular localization of glutamine synthetase (GS) in the inferior temporal cortices of non-demented elderly individuals was compared with that in brains affected by Alzheimer's disease (AD). The present study confirmed previous reports of a general decrease in GS expression in astrocytes and the expression of GS in some neurons. Several new observations were made: the morphology of astrocytes is generally unaffected by the presence of plaques, GS labeling is present in some diffuse plaques and occasional neuritic plaques, whereas the overall density of astrocytes increases 1.4-fold in AD. In addition, the present study found that the reduction in GS expression is almost entirely due to a loss of GS from perisynaptic regions of the neuropil and from the astrocytic endfeet that normally abut cortical blood vessels. These changes implicate astrocytes in glutamate excitotoxicity and ammonia neurotoxicity. It is suggested that it may be more fruitful to regard AD not as a neuronal disease, but as a disorder of astrocyte-neuron interactions.

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“…A useful marker to visualize the somata of astroglial cells are antibodies recognizing the calcium-binding protein S100b (Van Eldik and Griffin, 1994). The detoxifying enzyme, glutamine synthetase, is also largely restricted to astroglial somata and might be revealed with polyclonal antisera (Hallermayer and Hamprecht, 1984) or monoclonal antibodies (Pike et al, 1996) allowing for anatomical studies of brain (Derouiche et al, 1996) and retina Hä rtig et al, 1995).…”

Section: Introductionmentioning

confidence: 98%